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Your search keyword '"Igoor, Sindhu"' showing total 10 results
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10 results on '"Igoor, Sindhu"'

2. Cellular heterogeneity of pluripotent stem cell-derived cardiomyocyte grafts is mechanistically linked to treatable arrhythmias

Author

Selvakumar, Dinesh, Clayton, Zoe E., Prowse, Andrew, Dingwall, Steve, Kim, Sul Ki, Reyes, Leila, George, Jacob, Shah, Haisam, Chen, Siqi, Leung, Halina H. L., Hume, Robert D., Tjahjadi, Laurentius, Igoor, Sindhu, Skelton, Rhys J. P., Hing, Alfred, Paterson, Hugh, Foster, Sheryl L., Pearson, Lachlan, Wilkie, Emma, Marcus, Alan D., Jeyaprakash, Prajith, Wu, Zhixuan, Chiu, Han Shen, Ongtengco, Cherica Felize J., Mulay, Onkar, McArthur, Jeffrey R., Barry, Tony, Lu, Juntang, Tran, Vu, Bennett, Richard, Kotake, Yasuhito, Campbell, Timothy, Turnbull, Samual, Gupta, Anunay, Nguyen, Quan, Ni, Guiyan, Grieve, Stuart M., Palpant, Nathan J., Pathan, Faraz, Kizana, Eddy, Kumar, Saurabh, Gray, Peter P., and Chong, James J. H.

Published
2024
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3. Development of new adeno-associated virus capsid variants for targeted gene delivery to human cardiomyocytes

Author

Kok, Cindy Y., Tsurusaki, Shinya, Cabanes-Creus, Marti, Igoor, Sindhu, Rao, Renuka, Skelton, Rhys, Liao, Sophia H.Y., Ginn, Samantha L., Knight, Maddison, Scott, Suzanne, Mietzsch, Mario, Fitzsimmons, Rebecca, Miller, Jessica, Mohamed, Tamer M.A., McKenna, Robert, Chong, James J.H., Hill, Adam P., Hudson, James E., Alexander, Ian E., Lisowski, Leszek, and Kizana, Eddy

Published
2023
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7. Cellular Heterogeneity of Pluripotent Stem Cell Derived Cardiomyocyte Grafts is Mechanistically Linked to Treatable Arrhythmias

Author

Selvakumar, Dinesh, primary, Clayton, Zoe E., additional, Prowse, Andrew, additional, Dingwall, Steve, additional, George, Jacob, additional, Shah, Haisam, additional, Chen, Siqi, additional, Hume, Robert D., additional, Tjahjadi, Laurentius, additional, Igoor, Sindhu, additional, Skelton, Rhys J.P., additional, Hing, Alfred, additional, Paterson, Hugh, additional, Foster, Sheryl L., additional, Pearson, Lachlan, additional, Wilkie, Emma, additional, Jeyaprakash, Prajith, additional, Wu, Zhixuan, additional, McArthur, Jeffrey R., additional, Barry, Tony, additional, Lu, Juntang, additional, Tran, Vu, additional, Bennett, Richard, additional, Kotake, Yasuhito, additional, Campbell, Timothy, additional, Turnbull, Samual, additional, Nguyen, Quan, additional, Ni, Guiyan, additional, Grieve, Stuart M., additional, Palpant, Nathan J., additional, Pathan, Faraz, additional, Kizana, Eddy, additional, Kumar, Saurabh, additional, Gray, Peter P., additional, and Chong, James J.H., additional

Published
2022
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10. Therapeutic silencing of miR-652 restores heart function and attenuates adverse remodeling in a setting of established pathological hypertrophy.

Author

Bernardo, Bianca C., Nguyen, Sally S., Winbanks, Catherine E., Xiao-Ming Gao, Boey, Esther J. H., Yow Keat Tham, Kiriazis, Helen, Ooi, Jenny Y. Y., Porrello, Enzo R., Igoor, Sindhu, Thomas, Colleen J., Gregorevic, Paul, Lin, Ruby C. Y., Xiao-Jun Du, and McMullen, Julie R.

Subjects
GENE expression, MICRORNA, HEART diseases, HYPERTROPHY, NUCLEIC acids
Abstract

Expression of microRNA-652 (miR-652) increases in the diseased heart, decreases in a setting of cardioprotection, and is inversely correlated with heart function. The aim of this study was to assess the therapeutic potential of inhibiting miR-652 in a mouse model with established pathological hypertrophy and cardiac dysfunction due to pressure overload. Mice were subjected to a sham operation or transverse aortic constriction (TAC) for 4 wk to induce hypertrophy and cardiac dysfunction, followed by administration of a locked nucleic acid (LNA)-antimiR-652 (miR-652 inhibitor) or LNA control. Cardiac function was assessed before and 8 wk post-treatment. Expression of miR-652 increased in hearts subjected to TAC compared to sham surgery (2.9-fold), and this was suppressed by ~95% in LNA-antimiR-652-treated TAC mice. Inhibition of miR-652 improved cardiac function in TAC mice (fractional shortening:29±1% at 4 wk post-TAC compared to 35±1% post-treatment) and attenuated cardiac hypertrophy. Improvement in heart function was associated with reduced cardiac fibrosis, less apoptosis and B-type natriuretic peptide gene expression, and preserved angiogenesis. Mechanistically, we identified Jaggedl (a Notchl ligand) as a novel direct target of miR-652. In summary, these studies provide the first evidence that silencing of miR-652 protects the heart against pathological remodeling and improves heart function. [ABSTRACT FROM AUTHOR]

Published
2014
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